Table 3.
Conditions from ambient air pollution/oxidative stress (no co-existing conditions reported)
| Reference | Pollutant exposure | Type of study | Respiratory condition of focus | Number of subjects | Types of analysed markers and results |
|---|---|---|---|---|---|
| Echazarreta et al., 2005 [45] |
Oxidative stress |
Randomised, double-blinded, L-PAF-controlled, crossover study |
Mild asthma |
6 females (6 males) |
PAF: no increase in systemic markers of oxidative stress in response to PAF as normally seen in acute asthma. L-PAF: no significant results. From PAF challenge, peripheral blood neutrophils fell at 5 min (P < 0.01) followed by rebound neutrophilia at 15 and 45 min (P < 0.001 each). Rrs (to 5.5 cm H2OL−1s−1 (SD = 0.4)) (P < 0.005) and AaPo2 (to 27.1 mmHg (SD = 2.8)) increased whereas Pao2 decreased (to 76.2 mmHg (SD = 2.1)) (P < 0.001 each) at 5 min. Heart rate increased (from 70 min (SD = 1.7) to 78 min (SD = 2.2) − 1) (P < 0.005) at 5 min.uLTE4 elimination increased markedly (to 2144 pgmg (SD = 845) − 1) (P < 0.02) at 120 min. From L-PAF challenge, there was a small increase in AaPo2 at 5 and 15 min (P < 0.01 each). There was also a mild decrease in Pao2 at 15 min (P < 0.01). |
| Brook et al., 2009 [46] |
Air pollution |
Randomised, double-blind study |
Respiratory/vascular health |
15 females (16 males) |
ET-1, CRP, and cytokines: no significant differential change. |
| Chen et al., 2015 [47] | Outdoor particulate matter: PM2.5 were 103 μg/m3. Indoor (air purified) PM2.5 concentration: 96.2 μg/m3 | Randomised, double-blind crossover study | Acute airway inflammatsion | 25 females (10 males) | Serum biomarkers – CRP, fibrinogen, P-selectin, MCP-1, IL-1β, TNF-α, IL-6, MPO, sCD40L, PAI-1, t-PA, D-dimer, |
|
|
|
|
|
|
Improvements in all inflammatory markers pre- vs post-air filtration except for CRP. |
| Kumarathasan et al., 2018 [48] |
Environmental air pollution exposure |
Randomised crossover study |
Airway inflammation |
52 (male and female ratio not specified; no sex-based significance) |
IL-1β, IL-2, IL-6: up-regulated with no mask on (filtered vs not filtered air). |
| Zhao et al., 2020 [49] |
PM2.5 pollution waves |
Randomised crossover trial |
Respiratory inflammation |
13 females (16 males) |
Increased ox-LDL and 8-isoPGF2α levels with pollution exposure, other markers (MDA, GPx1, EC-SOD) not significant. |
| Solomon et al., 2023 [50] | Natural aetiology (can be environment, allergic response to environment, etc.) | Institution-based cross-sectional study (random sampling) | Asthma | 164 females (127 males) | Eosinophilia: lacking levels associated with low type-2 asthma phenotype. |
8-isoPGF2α – 8-iso-ptostaglandin F2-alpha, AaPO2 – alveolar-arterial oxygen gradient, CRP – C-reactive protein, EC-SOD – extracellular superoxide dismutase, ET-1 – endothelin-1, GPx1 – glutathione peroxidase 1, IL-1β, IL-2, IL-6 – interleukin 1-beta, 2, and 6, L-PAF – lyso-platelet-activating factor, MCP-1 – monocyte chemoattractant protein-1, MDA – malondialdehyde, a marker of oxidative stress, MPO – myeloperoxidase, PAF – platelet-activating factor, PAI-1 – plasminogen activator inhibitor-1, PaO2 – partial pressure of oxygen in arterial blood, PM2.5 – particulate matter with a diameter of less than 2.5 micrometers, Rrs – respiratory system resistance, sCD40L – soluble CD40 ligand, SD – standard deviation,
TNF-α – tumor necrosis factor-alpha, t-PA – tissue plasminogen activator, uLTE4 – urinary leukotriene E4, x-LDL – oxidized low-density lipoprotein